People with osteoarthritis have increased cell deterioration nearest to damaged joint, study finds

TUESDAY, Jan. 17 (HealthDay News) -- A process linked to natural cell aging has now also been associated with knee osteoarthritis, researchers say.

Telomeres -- lengths of DNA on the ends of chromosomes, sometimes described as being like the plastic cap on a shoelace tip -- naturally shorten with age, but can also shorten due to sudden cell damage. Abnormally short telomeres have been found in some types of cancer and preliminary research has suggested that the average telomere length is also shortened in osteoarthritis.

In this new study, Danish researchers used new technology to closely examine the telomeres of cells taken from the knees of osteoarthritis patients who had joint replacement surgery.

The cells had abnormally shorted telomeres and the percentage of cells with ultra-short telomeres increased with proximity to the damaged area in the knee joint, according to the findings published in the Jan. 16 online edition of the journal Arthritis Research & Therapy.

"The telomere story shows us that there are, in theory, two processes going on in osteoarthritis. Age-related shortening of telomeres, which leads to the inability of cells to continue dividing and so to cell senescence [deterioration], and ultra-short telomeres, probably caused by compression stress during use, which lead to senescence and failure of the joint to repair itself," study leader Maria Harbo said in a journal news release.

"We believe the second situation to be the most important in osteoarthritis. The damaged cartilage could add to the mechanical stress within the joint and so cause a feedback cycle driving the progression of the disease," she added.